To study conditions of human primary growth failure, including the chondrodystrophies, to determine whether mitochondrial energy metabolism is defective in these conditions (defective oxidative phosphorylation has been found in human achondroplasia, and to define the enzymatic defects which may be present. To study the mechanisms of reaction and structure of mitochondria and purified enzyme preparations from normal and phosphorylation-deficient tissue culture cells and yeast as model systems to aid in our understanding of normal and abnormal oxidative energy metabolism in the human. To study the biological and enzymatic changes which occur during iron deficiency and during the recovery period after specific treatment to better define the biochemical deficiencies which exist and their treatment. To study the effects of cellular aging on mitochondrial function and integrity in animals and in human tissue culture cells.